COX-2 up-regulates VEGF-C and promotes lymphangiogenesis in human lung adenocarcinoma.

Overexpression of vascular endothelial growth factor-C is associated with lung adenocarcinoma

This suggests that VEGF-C promotes lymph node metastasis while being influenced by the strength of the VEGF-C autocrine loop, and the VEGF-C/VEGFR-3 ratio can be a useful predictor of lymph node metastasis in non-small cell lung cancer.

In non-small-cell lung cancer cells, VEGF-C/VEGFR-3 coexpression suggests an autocrine/paracrine loop responsible for a high proliferation rate in tumour cells.

Under hypoxic conditions an autocrine loop between VEGF-C/VEGFR-3 and HIF-1 alpha is possible in breast carcinoma and lung carcinoma but not in colorectal carcinoma cell lines.

HIF-1alpha and VEGF-C were over-expressed in non-small cell lung cancer.

PRL-3 induces microvascular and lymphatic vessel formation by facilitating VEGF and VEGF-C expression in lung cancer tissues

HuR expression in non-small cell lung cancer correlates with vascular endothelial growth factor-C expression and lymph node metastasis

VEGF-C and -D may play important roles in lymphangiogenesis and lymph node metastasis in lung adenocarcinoma.

VEGF-C induced lung lymphangiogenesis and promoted intralymphatic spread of metastases in the lung and formation of tumor emboli in the pulmonary arteries.

The overexpressions of VEGF-C and EGFR genes are closely related to lymph node metastasis. VEGF-C mRNA and EGFR mRNA are valuable biomarkers for early diagnosis, clinical prediction and prognosis for lung cancer.

RNAi-mediated silencing of VEGF-C inhibits non-small cell lung cancer progression by simultaneously down-regulating the CXCR4, CCR7, VEGFR-2 and VEGFR-3-dependent axes-induced ERK, p38 and AKT signalling pathways.

Downregulation of VEGF-C expression in lung and colon cancer cells decelerates tumor growth and inhibits metastasis via multiple mechanisms

Data shsow that VEGF-C expression is an independent prognostic factor of stage IIIa (N2) lung adenocarcinoma and squamous cell carcinoma.

The expression levels of STAT3, P-STAT3, and VEGF-C were higher in small cell lung cancer than in normal tissue; STAT3 and VEGF-C play important roles in the development of small cell lung cancers

High mRNA expression of VEGFC is associated with non-small-cell lung cancer.

Platelet-derived growth factor-A and vascular endothelial growth factor-C might induce intimal proliferation in pulmonary arteries and contribute to the development of pulmonary tumor thrombotic microangiopathy.

the variant genotypes of the VEGF -2578C/A polymorphism, but not the VEGF -634G/C polymorphism, was associated with lung cancer risk.

Tbeta10 human recombinant proteins promoted the expression of VEGF-C by activating AKT phosphorylation in lung cancer cell lines.

Radiation-induced activation of the PI3K/Akt/mTOR signaling pathway increases VEGF-C expression in lung cancer cells, thereby promoting endothelial cell proliferation.

a potential link between the upregulation of Syk and VEGF-C expression and lung adenocarcinoma.

Results has shown that VEGF-C was highly expressed in non-small cell lung cancer (NSCLC) tissues and metastatic lymph nodes. VEGF-C expression levels was significantly correlated with lymph node metastasis in NSCLC. Along with CXCR4, VEGF-C might synergically promote lymphatic metastasis in lung cancer and might be a clinical predictor of lymph node metastasis in NSCLC patients.

Clinical importance of VEGFC and PD-L1 co-expression in lung adenocarcinoma patients.

tumor-derived VEGF-C draining to regional lymph nodes promotes the outgrowth of lymph node metastases. VEGF-C may induce lung metastasis independently of its effects on lymph node metastasis.